The effects of boldine [(S)-2,9-dihydroxy-1,10-dimethoxyaporphine], a major alkaloid in the leaves and bark of boldo (Peumus boldus Mol.), on skeletal muscle were studied using mouse diaphragm and isolated sarcoplasmic reticulum membrane vesicles. Boldine, at 10-200 μM, has little effect on the muscle-evoked twitches; however, the ryanodine-induced contracture was potentiated dose-dependently. At higher concentrations of 300 μM, boldine by itself induced muscle contracture of two phases, which were caused by the influx of extracellular Ca2+ and induction of Ca2+ release from the internal Ca2+ storage site, the sarcoplasmic reticulum, respectively When tested with isolated sarcoplasmic reticulum membrane vesicles,boldine dose-dependently induced Ca2+ release from actively loaded sarcoplasmic reticulum vesicles isolated from skeletal muscle of rabbit or rat which was inhibited by ruthenium red, suggesting that the release was through the Ca2+ release channel, also known as the ryanodine receptor. Boldine also dose-dependently increased apparent [3H]-ryanodine binding with the EC50 value of 50 μM. In conclusion, we have shown that boldine could sensitize the ryanodine receptor and induce Ca2+ release from the internal Ca2+ storage site of skeletal muscle.

Original languageEnglish
Pages (from-to)18-21
Number of pages4
JournalPlanta Medica
Issue number1
Publication statusPublished - 1998


  • Boldine
  • Ca release
  • Monimiaceae
  • Peumus boldus
  • Sarcoplasmic reticulum

ASJC Scopus subject areas

  • Drug Discovery
  • Analytical Chemistry
  • Molecular Medicine
  • Complementary and alternative medicine
  • Pharmacology
  • Pharmaceutical Science
  • Organic Chemistry


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